Cell state · L2
EPI.renal_intercalated_cell_type_B.baseline
409 cells in the full atlas (not the displayed sample).
These are the cell-population annotations shown in the SCREATE Cell Browser.
Read trait, study and gene evidence reports for this population →
Explore this population in Cell Browser →
Marker genes
ATP6V0A4, ATP6V1B1, ATP6V1G3, CA12, CDA, FOXI1, INSRR, KRTAP5-8, MAG, MMD, NTRK1, OXCT1, SLC26A4, SLC4A9, WDR72
Annotation genes
ATP6V0A4, ATP6V1B1, CA12, FOXI1, SLC26A4, SLC4A9
Annotation rationales
Classic B-IC identity is defined by pendrin (SLC26A4), the apical Cl⁻/HCO₃⁻ exchanger that secretes bicarbonate into the tubular lumen, and AE4 (SLC4A9) on the basolateral membrane to recycle HCO₃⁻/Cl⁻. Multiple V-ATPase subunits (ATP6V0A4, ATP6V1B1, ATP6V1G3) support basolateral H⁺ extrusion, the hallmark polarity of B-ICs (opposite of A-ICs). CA12 supplies rapid CO₂↔HCO₃⁻ conversion at the membrane, and FOXI1 is the lineage TF for IC differentiation. WDR72 (V-ATPase trafficking/acidification) and OXCT1 (ketone/acid–base metabolism) further support active bicarbonate handling. Expanded: sensory inputs (INSRR/NTRK1) likely tune bicarbonate secretion to volume/alkali status.
Functional implications
Fine control of acid–base and chloride balance in the cortical collecting system: drives luminal HCO₃⁻ secretion and Cl⁻ reabsorption, buffers systemic alkalosis, and supports aldosterone/volume-responsive Cl⁻ salvage in concert with principal cells. Maintains appropriate tubular pH to protect epithelium and modulates transport set-points during dietary salt/alkali loads or recovery from acid–base disturbances.
Marker and functional descriptions are atlas annotations. Explore gene expression, trait associations and regulatory elements in the interactive browsers; see the browser guide.